The review focuses on the value of the type I and III interferon (显示 IFNA 抗体) subtypes (alphas, beta and lambdas) as therapeutics for prevention and treatment of viral infections (influenza, herpes, human immunodeficiency virus and hepatitis viruses).

This review briefly discusses the dysregulation of main T cell subpopulations in CNS autoimmunity and summarized the T cell targeted effects of endogenous and exogenous IFN-beta in health and EAE/MS, with emphasis on the direct actions of IFN-beta on each T cell subset involved in the disease.

results suggest that, in addition to its well-known signaling activity, IFN-beta may be directly antimicrobial and be part of a growing family of cytokines and chemokines, called kinocidins, that also have antimicrobial properties.

This review briefly discusses the dysregulation of main T cell subpopulations in CNS autoimmunity and summarized the T cell targeted effects of endogenous and exogenous IFN-beta in health and EAE/MS, with emphasis on the direct actions of IFN-beta on each T cell subset involved in the disease.

Rb selectively inhibits innate IFN-beta production by enhancing deacetylation of Ifnb1 promoter, exhibiting a previous unknown non-classical role in innate immunity, which also suggests a role of Rb in the regulation of type I IFN production in inflammatory or autoimmune diseases.

The data demonstrate that an atypical TLR7 (显示 TLR7 抗体) signaling pathway contributes to type interferon-beta expression during Y. pestis infection and suggest that the TLR7 (显示 TLR7 抗体)-driven type I IFN response plays an important role in determining the outcome of plague.

The data confirm the involvement of EHMT2 (显示 EHMT2 抗体) in the epigenetic regulation of IFN-b and demonstrate the activation of a general antiviral state after EHMT2 (显示 EHMT2 抗体) inhibition.

The authors provide evidence that ICP27 protein encoded by bovine herpesvirus type 1, a viral early protein that shuttles between the nucleus and cytoplasm inhibits transcriptional activity of two bovine IFN-beta gene promoters (IFN-beta1 and IFN-beta3).

Overall, data provide evidence for the possible role of PI3K in the activation of the transcription of IFN-alpha (显示 IFNA 抗体)/beta by PRRSV; study concludes that PRRSV inhibits the induction of IFN-alpha (显示 IFNA 抗体) in monocyte-derived dendritic cells by as yet undefined post-transcriptional mechanisms.